Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Placenta-derived chymotrypsin-like protease (CLP/chymase) promotes endothelial P-selectin and E-selectin expression, which may be responsible for the increased neutrophil/endothelial interactions in preeclampsia (PE). However, little is known about this protease expression and production in human placenta. This study was undertaken to determine the distribution and gene expression of CLP in human placenta. Human placental tissues were obtained immediately after delivery from normal and PE pregnancies. We examined (1) CLP/chymase immunoactivity by immunohistochemical staining of villous tissue sections; (2) trophoblast mRNA and protein expression for chymase by RT-PCR and Western blot analysis; (3) chymase cDNA sequencing in isolated trophoblast cells (TCs); and (4) release of CLP by placental villous tissue cultured under 2% and 20% O(2). We found (1) CLP expression is mainly localized in the epithelial layer of syncytiotrophoblasts; (2) both mRNA and protein expression are significantly (p<0.05) upregulated in TCs isolated from PE vs. normal placentas; (3) TC chymase cDNA sequence and the deduced amino acid sequence are 100% identical to that reported for the human heart; and (4) villous tissue releases more chymotrypsin when cultured with 2% O(2). We conclude that (1) the DNA and protein sequence for chymase in placental trophoblast cells are the same as those reported in the human heart; (2) CLP/chymase expression is upregulated in TCs during PE; and (3) lowered oxygen condition promotes CLP release by placental TCs. Since chymase is a potent non-ACE angiotensin II producing enzyme, our data suggest that if placenta-derived CLP/chymase is released into the maternal circulation, it may contribute to the cardiovascular complications associated with PE.
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PMID:Increased chymotrypsin-like protease (chymase) expression and activity in placentas from women with preeclampsia. 1669 79

Forty five smokers were classified into schistosomal cases with type-2 diabetis mellitus (GI) and with associated history of bronchial asthma (GII) and without T-2 DM (GIII). A control group (GIV) of non-diabetic non schistosomal age matched subjects who quitted smoking for >6 months were included. Assessed parameters included indices of glycemic status (glycated hemoglobin), angiogenesis (vascular endothelial growth factor) hepatic and bronchoalveolar disposition (Liver function test, metallothionein, serum levels of cotinine, cadmium selenium, copper & zinc) and bronchoalveolar lavage) (BAL) levels of surfactant proteins A & D, zinc and copper oxidative stress and fibrogenesis (total antioxidant capacity thiobarbituric acid reactive substance) and vasculopathy (angiotensin converting enzyme, P-selectin, nitrate) and periodontitis (collagenase and elastase in GCF) impact of cigarette smoking associated with trace element disbalance and enzymatic changes in crevicular fluid on altered parameters collaborative out-come. The study reflected the collaborative outcome of immune mediated mechanisms initiated by liver affection, glycemic status and history of predisposed bronchial integrity induced by oxidative stress.
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PMID:Cigarette smoking induced liver insult concomitant with inflammatory mediators in serum crevicular fluid and bronchio alveolar lavage of schistosomal diabetic subjects with history of bronchial asthma. 1792 10


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